FFS: Amaurosis fugax

Amaurosis fugax is considered a form of anterior circulation TIA, involving acute transient monocular vision loss due to retinal ischemia.

The term is sometimes used more broadly for any transient visual loss, but this is clinically unhelpful. For the purposes of this draft, it refers specifically to vascular pathology causing monocular vision loss.

It is classified as high-risk due to:

• Strong association with high-grade carotid stenosis
• Risk of subsequent stroke
• Risk of recurrent visual loss leading to permanent blindness

All cases warrant urgent stroke specialist review and investigation.

History

The term comes from Greek “amaurosis” (darkness) and Latin “fugax” (fleeting) — “fleeting darkness”.

In the early 1800s, amaurosis fugax merely meant loss of sight and by the 1830s, was used to describe fleeting blindness, regardless of laterality or aetiology. In the early 1900s, the term ‘transient monocular blindness’ was used interchangeably with amaurosis fugax.  In 1993 Charles Miller Fisher (1913-2012)helped to define the term we use today in his paper ‘Transient monocular blindness’ versus ‘amaurosis fugax‘

Pathology

Common causes:

• Emboli from carotid artery disease (most common)
• Emboli from cardiac sources
• Emboli from internal carotid or ophthalmic artery (uncommon)
• Transient hypoperfusion from stenosis

Uncommon causes:

• Procoagulant disorders
• Vasculitis, especially giant cell arteritis (age > 50)
• Migrainous vasospasm

Monocular vs binocular visual loss

• Monocular: pathology anterior to optic chiasm — retina or optic nerve (amaurosis fugax)
• Binocular: pathology posterior to optic chiasm — vertebrobasilar TIA or migraine

Clinical assessment

Key history features:

• Monocular vision loss, described as partial or total, fogging to blackness
• Painless if embolic; painful episodes suggest migraine, glaucoma, or giant cell arteritis
• Transient: usually seconds to minutes, occasionally hours
• CVS risk factors: diabetes, hypertension, dyslipidaemia, smoking, PVD

Examination:

• Document visual acuity
• Assess for visual field defects
• Fundoscopy: may show embolus in retinal arteriole
• Assess for embolic source: AF, murmurs, carotid bruits

Differential diagnoses

• Optic neuritis (e.g. MS)
• Vitreous floaters
• Migraine variants
• Transient central retinal vein occlusion

Investigations

Blood tests:

• FBC
• U&Es / glucose
• ESR / CRP (vasculitis, GCA)
• Coagulation studies
• Lipid profile

ECG:

• Especially for AF

Carotid Doppler Ultrasound:

• Screen for carotid stenosis

CT head / CT angiogram:

• CT excludes intracerebral bleed
• CT angiogram visualises carotid and vertebrobasilar vasculature

MRI / MRA:

• Best modality for visualising cerebral vasculature
• Use if CT angiogram contraindicated

Echocardiography:

• Consider in younger patients or if embolic source suspected

Management

1. Antiplatelet therapy:
   • Aspirin, clopidogrel, or Asasantin (aspirin + dipyridamole)
2. Anticoagulation:
   • Consider if crescendo symptoms, AF, or cardiac embolic source
   • Bridge with heparin or enoxaparin where appropriate
3. Control cardiovascular risk factors
4. Surgical management:
   • Carotid endarterectomy for moderate (50–70%) or high-grade (>70%) stenosis

Disposition

• Admit to stroke unit or short stay with neurology review
• Refer to vascular surgery for significant carotid stenosis
• Ophthalmology review if diagnosis uncertain

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References

Publications

• Fisher CM. ‘Transient monocular blindness’ versus ‘amaurosis fugax’. Neurology. 1989 Dec;39(12):1622-4.
• Kaur K, Najem K, Margolin E. Amaurosis Fugax. 2025 Jan 21. In: StatPearls 

FOAMed

• Nickson C. I can see clearly now. LITFL